title: Endovascular cooling and endothelial activation in hemorrhagic stroke patients.
abstract: BACKGROUND
  Little is known about endothelial activation under the influence of endovascular temperature management. This analysis was designed to measure the endothelial markers Angiopoietin-1 (Ang-1) and -2 (Ang-2) in endovascularly based prophylactic normothermia versus conventional temperature management.
  
  
  METHODS
  In this randomized controlled trial patients with spontaneous subarachnoid or spontaneous intracerebral hemorrhage were prospectively enrolled and randomized in two treatment arms: (a) prophylactic normothermia group with target core temperature 36.5°C using endovascular cooling, (b) active control group with conventional stepwise predefined fever management using antipyretic medication and surface cooling. Blood samples were obtained on days 1, 4, and 7. In a substudy Ang-1 and -2 were measured in 63 patients for whom samples on consecutive days were available.
  
  
  RESULTS
  The median total fever burden during the course of treatment was 0.0°C and 5.9°C h in the endovascular and the conventional group, respectively (P < 0.0001). Angiopoietin serum levels did not yield a statistical difference when comparing the two treatment arms. Ang-1 was significantly lowered, whereas Ang-2 levels were significantly elevated on day 4 compared to baseline levels irrespective of group allocation (P < 0.0001). The application of non-steroidal anti-inflammatory drugs (NSAIDs) was associated with significantly increased Ang-1 (P < 0.05) and lower Ang-2 levels on day 7 (P < 0.05).
  
  
  CONCLUSIONS
  Endovascular long-term temperature management did not alter Ang-1 and -2 levels compared to the control group indicating that the endovascular cooling technique itself does not lead to additional endothelial impairment. However, application of NSAIDs led to lower Ang-2 serum concentrations in the endovascular group.
authors.affiliation: Department of Neurology, Neurologic Intensive Care Unit, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria.
authors.forename: Marlene
authors.initials: M
authors.lastname: Fischer
authors.forename: Anelia
authors.initials: A
authors.lastname: Dietmann
authors.forename: Peter
authors.initials: P
authors.lastname: Lackner
authors.forename: Ronny
authors.initials: R
authors.lastname: Beer
authors.forename: Raimund
authors.initials: R
authors.lastname: Helbok
authors.forename: Bettina
authors.initials: B
authors.lastname: Pfausler
authors.forename: Markus
authors.initials: M
authors.lastname: Reindl
authors.forename: Erich
authors.initials: E
authors.lastname: Schmutzhard
authors.forename: Gregor
authors.initials: G
authors.lastname: Broessner
mesh_terms: D000328:Adult; D000368:Aged; D042683:Angiopoietin-1 / Q000378:metabolism; D042702:Angiopoietin-2 / Q000378:metabolism; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D015415:Biomarkers / Q000378:metabolism*; D001831:Body Temperature; D002543:Cerebral Hemorrhage / Q000150:complications / Q000378:metabolism / Q000628:therapy; D017679:Cryotherapy / Q000379:methods*; D004730:Endothelium, Vascular / Q000378:metabolism*; D057510:Endovascular Procedures / Q000379:methods; D005260:Female; D005334:Fever / Q000209:etiology / Q000378:metabolism / Q000628:therapy*; D006801:Humans; D020300:Intracranial Hemorrhages / Q000150:complications / Q000378:metabolism / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000378:metabolism / Q000628:therapy
chemical_list: C467630:ANGPT1 protein, human; D042683:Angiopoietin-1; D042702:Angiopoietin-2; D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers